Abstract

During reperfusion of a myocardial infarct, development of microvascular occlusion may result in regional hypoperfusion (“no reflow”) despite a patent infarct-related artery. This study examined the extent and time course of no reflow with use of rubidium-82 positron emission tomography. In 12 anesthetized dogs, the left anterior coronary artery was occluded for 90 min and then freely reperfused. Regional myocardial perfusions was imaged by serial rabidium-82 positron emission tomography during coronary occlusion and every 30 min during reperfusion. After 4 h of reperfusion, infarct size and no reflow zone were measured postmortem by triphenyltetrazolium and thioflavin staining, respectively.

Perfusion defects evident on rubidium-82 images during coronary occlusion rapidly resolved during the early reflow period. However, a recurrent perfusion defect appeared after 1 to 2 h of reflow in all dogs. The severity of recurrent perfusion defects progressed with time; after 5 min of reflow, relative perfusion in the left anterior descending artery territory was 97 ± 6% of that in the normal circumflex artery region, but perfusion decreased progressively to 68 ± 5% after 2 h (p < 0.05) and to 55 ± 4% after 4 h of reperfusion (p < 0.05 versus 2 h). As measured by radioactive tracer microspheres, endocardial blood flow decreased similarly in the postischemic left anterior descending artery region from 1.2 ± 0.2 ml/mim per g after 5 min of reflow to 0.4 ± 0.1 ml/min per g after 3 h of reflow (p < 0.01). Residual infarct perfusion, measured by rabidium-82 after 4 h of reflow, was related to both infarct size (r = −0.88) and the extent of the no reflow zone (r = −0.84) in the postmortem left ventricular sections.

Thus, serial positron emission tomography with rabidium-82 demonstrates a progressive loss of infarct perfusion, beginning 1 to 2 h after initial restoration of blood flow despite patency of the infarct-related artery. This phenomenon is probably a manifestation of progressive microvascular occlusion within the reperfused myocardium.

Footnotes

↵1 Dr Jeremy is an Overseas Research Fellow of the National Heart Foundation of Australia, Canberra. Australian Capital Territory, Australia and recipient of a Telectronics Overseas Fellowship from the Royal Australasian College of Physicians, Sydney, New South Wales, Australia.

☆ This work was supported by U.S. Public Health Service Grants 17655-15 (SCOR in Ischemic Heart Disease) and R01 33360 from the National institutes of Health, Bethesda, Maryland. Support was also received from Squibb Diagnostics, New Brunswick, New Jersey.

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